{"title":"030 Brain aging and cardiovascular risk factors in chronic HIV: A longitudinal MRI study","authors":"D. Jakabek, C. Rae, B. Brew, L. Cysique","doi":"10.1136/bmjno-2021-anzan.30","DOIUrl":null,"url":null,"abstract":"Objectives We aimed to examine the relative contributions of HIV infection, age, and cardiovascular risk factors to subcortical brain atrophy. Methods Virally suppressed HIV+ participants with low neuropsychological confounds (n = 75) and demographically matched HIV- controls (n = 31) completed baseline and 18-month follow-up MRI scans, neuropsychological evaluation, cardiovascular assessments, and laboratory tests. HIV+ participants were evaluated for HIV associated neurocognitive disorder (HAND). Subcortical volumes were extracted with Freesurfer. Volumetric and shape analyses were conducted using linear mixed-effect models incorporating interactions between age, time, and each of HIV status, HAND status, HIV disease factors, and cardiovascular markers. Results HIV+ participants had smaller volumes of most structures compared to HIV- participants. Premature aging was evident in the pallidum using volumetric (p = 0.032) and shape analyses. Accelerated aging was observed in the caudate volumes for the more severe HAND subgroup (p = 0.008) and was associated with longer HIV duration for putamen volumes (p = 0.04). Higher CD4 counts had a protective effect on hippocampal volumes in older participants (p = 0.04). Cardiovascular measures were associated with smaller volumes across time for most structures; only the putamen demonstrated accelerated atrophy over time in HIV+ participants with higher cardiovascular risk factors (p = 0.002). Conclusion The study demonstrates a three-hit model of subcortical injury in HIV+ individuals: HIV-driven atrophy in most subcortical structures; abnormal brain aging and HIV infection synergy in the caudate and pallidum; and cardiovascular-related injury linked to diffuse premature atrophy and emerging accelerated atrophy in the putamen.","PeriodicalId":19692,"journal":{"name":"Oral abstracts","volume":"10 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral abstracts","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1136/bmjno-2021-anzan.30","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objectives We aimed to examine the relative contributions of HIV infection, age, and cardiovascular risk factors to subcortical brain atrophy. Methods Virally suppressed HIV+ participants with low neuropsychological confounds (n = 75) and demographically matched HIV- controls (n = 31) completed baseline and 18-month follow-up MRI scans, neuropsychological evaluation, cardiovascular assessments, and laboratory tests. HIV+ participants were evaluated for HIV associated neurocognitive disorder (HAND). Subcortical volumes were extracted with Freesurfer. Volumetric and shape analyses were conducted using linear mixed-effect models incorporating interactions between age, time, and each of HIV status, HAND status, HIV disease factors, and cardiovascular markers. Results HIV+ participants had smaller volumes of most structures compared to HIV- participants. Premature aging was evident in the pallidum using volumetric (p = 0.032) and shape analyses. Accelerated aging was observed in the caudate volumes for the more severe HAND subgroup (p = 0.008) and was associated with longer HIV duration for putamen volumes (p = 0.04). Higher CD4 counts had a protective effect on hippocampal volumes in older participants (p = 0.04). Cardiovascular measures were associated with smaller volumes across time for most structures; only the putamen demonstrated accelerated atrophy over time in HIV+ participants with higher cardiovascular risk factors (p = 0.002). Conclusion The study demonstrates a three-hit model of subcortical injury in HIV+ individuals: HIV-driven atrophy in most subcortical structures; abnormal brain aging and HIV infection synergy in the caudate and pallidum; and cardiovascular-related injury linked to diffuse premature atrophy and emerging accelerated atrophy in the putamen.